Larsen P R, Frumess R D
Endocrinology. 1977 Apr;100(4):980-8. doi: 10.1210/endo-100-4-980.
To compare the biological effects of thyroxine (T4) and triiodothyronine (T3), the results of varying the production rates of T3 and T4 independently were evaluated. In one set of experiments, the responses of hypothyroid rats to thyroid hormones were measured in terms of weight gain, hepatic mitochondrial alpha-glycerophosphate dehydrogenase (alphaGPD) and serum TSH. T4 was given with, and without, 6-n-propylthiouracil (PTU) and alphaGPD activity paralleled, and could completely be accounted for, by the effect of the quantities of the T3 produced. The direct role of T3 production in the maintenance of hepatic alphaGPD activity was supported by finding normal serum T3 and alphaGPD activities, but reduced T4, in rats on low iodine diet for 2 months. Only after 4 months of iodine deficiency was alphaGPD reduced in the presence of a normal serum T3. These results suggest that T4 per se plays minimal role in this system. In contrast, there were significant effects of T4 administration on stimulation of weight gain and suppression of TSH release in hypothyroid animals which were not due to the T3 produced by peripheral conversion. While T3 given parenterally was about tenfold more potent than T4 in acute suppression of TSH, PTU retreatment did not alter the acute decrease in TSH after T4 which lasted for at least 22 h, as opposed to less than 7 h for T3. Despite the direct effect of T4 on TSH suppression , acute reduction in T3 in normal rats resulted in an elevation of serum TSH even though serum T4 concentrations were unchanged or even increased at this time. The results indicate that the thyrotroph, unlike the hepatocyte, can respond acutely to both increases and decreases in either T3 or T4 production. The differential sensitivities of various tissues to T3 and T4 indicate that the relative potencies of these two hormones must be defined experimentally in terms of a specific biological effect.
为比较甲状腺素（T4）和三碘甲状腺原氨酸（T3）的生物学效应，对独立改变T3和T4生成率的结果进行了评估。在一组实验中，以体重增加、肝线粒体α-甘油磷酸脱氢酶（αGPD）和血清促甲状腺激素（TSH）为指标，测定了甲状腺功能减退大鼠对甲状腺激素的反应。给予T4时，无论有无6-正丙基硫氧嘧啶（PTU），αGPD活性均与所产生的T3量的效应平行，且完全可由其解释。低碘饮食2个月的大鼠血清T3和αGPD活性正常，但T4降低，这支持了T3生成在维持肝αGPD活性中的直接作用。仅在碘缺乏4个月后，血清T3正常时αGPD才降低。这些结果表明，T4本身在该系统中作用极小。相反，给予T4对甲状腺功能减退动物的体重增加刺激和TSH释放抑制有显著作用，这并非外周转化产生的T3所致。虽然经胃肠外给予T3在急性抑制TSH方面比T4强约10倍，但再次给予PTU并未改变T4给药后TSH至少持续22小时的急性下降，而T3给药后TSH急性下降持续不到7小时。尽管T4对TSH抑制有直接作用，但正常大鼠T3急性降低导致血清TSH升高，即使此时血清T4浓度未变甚至升高。结果表明，与肝细胞不同，促甲状腺细胞对T3或T4生成的增加和减少均可产生急性反应。各种组织对T3和T4的不同敏感性表明，必须根据特定生物学效应通过实验来确定这两种激素的相对效力。
